Why the MCAT Bio / Biochem section is so critical and how to read a passage, Part I
Medicine is cool because it’s humble. Practitioners realize they don’t know everything. However, they continue to toil because doctors have an unwavering loyalty to the only method that matters: the scientific one. It’s been pretty much the greatest framework for scholarship ever conceived by man and we owe our impressive progress as a species to our disciplined adherence to the method. So, doctors need fluency with the technical literature because it’s an established conduit for new advances. After all, in order to treat patients better, physicians need to be armed with the latest and greatest research. My really great MCAT tutor started a journal club to help sharpen that evaluative skill so that we could achieve stratospheric results on the real MCAT. Today, in addition to currently producing a medical documentary on Parkinson’s disease, I would like to continue that tradition by doing a deep-dive on how one should proceed through a dense passage that is typical of what you would find on the real deal.
These tips aren’t easy, because I want to write for those with ambitions to be a competitive applicant for top med schools and have their sights sets on attaining a score in the upper echelon (515+). If you’re OK with being average, please do not read this blog. I want to reach the dedicated people who ask themselves every time they sit down to study for the MCAT, “If Michael Phelps or LeBron James were studying for the MCAT, would he be doing this? Would this be on his agenda?” The idea behind this is obvious: if you want a superstar score, you need superstar habits.
Tip 1: Try to understand every word
I know this flies in the face of conventional logic, but I’ve seen hundreds of students (including myself) continue to miss a substantial number of questions simply because of a passage misinterpretation. Skimming leads to mistakes, at least for me, so I’m going to use 4–5 minutes of the 8 minutes I have to tackle an MCAT passage to completely absorbing myself in that passage. As I learned in journal club, the questions become painfully obvious once I’ve understood the purpose — literally, the MAIN IDEA — of the entire investigation.
I want to start with this tip because I go into instant panic mode when I see a particularly challenging passage. If you were to track my eyeballs while encountering an abstruse MCAT passage, it would look like I was watching a tennis match at 100x normal speed — they are constantly darting back and forth like I’m nystagmic. This is because I used to pray that if I simultaneously read the passage and questions over and over again quickly, eventually the answer will pop in my head. This is wishful thinking. There’s an organized and logical way to tackle these MCAT passages, and while you’re trying to understand every word…
Tip 2: Take succinct but copious notes on the passage
“But, Arjan, won’t my hands cramp? Do I have time to take a ton of notes while trying to understand the passage?” That’s a horrendous excuse to not work hard. I don’t have time for babies, so if this is you, please close out of my blog and peruse something else. If you’re ever about to make an excuse not to do something, just ask yourself: how would a pre-med Michael Phelps do this? To get a superstar score, what do you need?
Let me tell you something: by the time the real MCAT rolls around, you won’t actually be taking copious notes. Why? Because by that time, you will have surreptitiously built your working memory capacity to the point where you won’t need to take many notes to understand the passage. But while you actually are practicing, you need to struggle and be super stressed by time constraints and actually build that mental muscle and stamina.
So let’s try a passage:
I really loved textbooks that spoke to me in a conversational style, so when I say take copious notes, I’m actually saying recast the technical language and words into informal, easy to understand facts. Here’s how I would re-phrase this passage:
Paragraph 1: Endometrial carcinomas (ECs) kill because they spread. Before we treat it, we need to understand it.
Quick pro-tip: your notes should say EC to save time, but when you read it with your inner voice, you should say the full name of endometrial carcinomas so you don’t forget what it stands for and spend time looking back at the passage hunting it down.
Paragraph 2: MSCs ↑ ⟼ Spreadability ↑ & Tumor growth ↑.
See how much information is packed into this tiny mathematical-style relationship? “High proliferative capacity” is a fancy phrase for can spread easily. This mathematical notation allows you to easily trace how changes propagate down a pathway. I put an up-arrow next to MSCs because it’s a convenient shorthand for, “the more MSCs I have, the more migration we see and the more the tumor will grow.
Next, the passage implicates a Sushi transmembrane protein in tumorigenesis and proliferation — literally just synonyms of tumor growth and spreadability.
Paragraph 2:
MSCs ↑ ⟼ Spreadability ↑ & Tumor growth ↑.
Cancer: MSCs ↑ ⟼ MSC marker = SUSD2 ↑ ⟼ Spreadability ↑ & Tumor growth ↑.
Finally, we incorporate the information about TGFß: TGFß ↑ ⟼ SUSD2 ↓. The beauty with these relationships is that I can easily see how an increase of the inhibitor should lead to a decrease in spreadability and tumor growth — or in the argot of the passage: decreases proliferation and tumorigenesis. The idea is that you won’t have to return to the passage, since everything important is already captured by your notes.
Your final paragraph annotation should look like:
Paragraph 2:
MSCs ↑ ⟼ Spreadability ↑ & Tumor growth ↑.
Cancer: MSCs ↑ ⟼ MSC marker = SUSD2 ↑ ⟼ Spreadability ↑ & Tumor growth ↑.
TGFß ↑ ⟼ SUSD2 ↓
Now paragraph 3 leads us to the next tip…
Tip 3: Always, always, always draw a picture
Paragraph 3 was likely written by someone who is trying to succinctly describe a diagram they drew for a paper. Your job is to reverse engineer that drawing by illustrating it one sentence at a time. There’s literally an art to it:
This is the TGFß pathway illustrated. Notice how I have a ligand approaching an active site with the Ser and Thr residues that phosphorylate SMADs 2 and 3 before hooking up with SMAD 4 and posting up in the nucleus to start running things in the cell, like proliferation (“Prolif.”), apoptosis (“Apop.”), and differentiation (“∂’ntion”). The idea, again, is to never have to revisit paragraph 3 again. Any wrenches to the pathway a question could throw my way will simply be “applied” to the drawing. What I mean is that say a question discusses treatment of your carcinomas with a substance that blocks SMAD4. We can easily trace how this change propagates through this signaling pathway: without SMAD4, you can’t link up with your phosphorylated SMADs 2 and 3 to translocate to the cell’s control center.
My tutor showed me the power of drawing after we timed how long I took to answer simple passage questions about a process being described. I learned I didn’t have the working memory capacity to keep all the “computational” overhead I was accumulating straight: I would start forgetting stuff immediately after reading the next sentence not being able to see how the two connected and would waste precious time re-reading. Illustrations completely changed that, and I wouldn’t have been able to perform well on the MCAT without cultivating that skill.
By now, it should be pretty evident why I annotated the next paragraph’s first few sentences as follows (try it before you continue forward; if you don’t try it, you’re a slacker lol):
Paragraph 4:
Aging ↑ ⟼DNA damage↑ ⟼ Apoptosis ↑ OR Senescence ↑
Senescence ↑ ⟼ SMAD 2/3 ↑ ⟼ Proliferation / Apoptosis / Differentiation Regulation ↑
It’s easy to get lost in the details and lose sight of the big picture, but remember, we are trying to figure out how proliferation occurs so we know how to treat it (paragraph 1). Do these types of cancers spread because an over-expression of MSC markers helps it proliferate? We see that in this paragraph, researchers want to know: what happens to our SMADs when we knockout our transmembrane marker, SUSD? So they applied an siRNA to stymie expression of SUSD. Notice how I said that Proliferation, Apoptosis, and Differentiation Regulation rose with SMAD 2/3 because:
SMAD 2/3 ↑ ⟼ SMAD 2/3 hooking up with SMAD 4↑ ⟼translocating to the nucleus ↑ ⟼ Proliferation / Apoptosis / Differentiation Regulation ↑
It’s overkill, but at least you won’t have to look back at the passage.
Tip 4: Understand every figure completely because if you can’t interpret data, you won’t be able to answer a single question
One of my good friends from this past summer whom I had the pleasure to study for the MCAT with noticed his score began rising spectacularly as soon as he took a breath each time he saw a complicated graph and mentally “stepped back” from being absorbed in the exam as if experiencing an out-of-body episode to ask himself, “OK, what’s being asked here?” Well, in this case, researchers blocked SUSD expression in order to see how SMADs were affected, remember? So we see that there’s a statistically significant difference between control and the experimental group: recall how the p-value illustrates the probability that the difference between treatments (experimental v. control) was entirely due to chance is less than 0.01%! This is extremely significant: when the passage authors silenced SUSD, SMAD 2/3 expression cratered. So now we know that:
Figure 1: SUSD ↓ ⟼ SMAD 2/3 ↓
Finally, we reach the last paragraph and figure (I combine the annotation to make the relationships clearer):
Paragraph 5 + Figure 2:
Expt. 1 — TGFß ↑ ⟼ apoptosis ↑
How did I know this? Literally, figure 2’s caption (sub G0-G1 = apoptosis)! This is a good time to remind you that every single word is important! If you had skimmed over the caption, you would have missed this crucial, juicy bit of information. Onto the other experiment in this second phase, where we knocked SUSD out again.
Expt. 2 — SUSD ↓ ⟼ apoptosis ↑
Let’s put everything together and see if we can explain the whole experiment as informally as possible using the results we just read off the graphs:
Certain tumors kill because they can spread easily. We noticed they can spread thanks to a key protein that almost always accompanies the cancer called SUSD, and which is inhibited by a growth factor (TGFß). When we KO’d SUSD, we got fewer SMADs, which are proteins that turn up in senescent cells. SMADs enter the picture when TGFß binds, and we see more apoptosis in Expt. 1 of the second pair of experiments (last paragraph) when we administered the growth factor. In Expt. 2 of that second pair, when we KO’d SUSD, we saw a rise in apoptosis.
And that’s the experiment, ladies and gentlemen! With this level of analysis on the passage, you will be able to quickly answer nearly any question they throw your way.
Don’t believe me? Tune in to the next installment, where I go over the questions associated with this passage so you can see just how much easier of a time you’ll have once you’ve mastered the passage.
Update: Part II is available here!
